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Paraspinal Muscles and Intervertebral Dysfunction: Part One
REVIEW OF LITERATURE PARASPINAL MUSCLES AND INTERVERTEBRAL DYSFUNCTION: PART ONE Gary Fryer, BAppSc(Osteo),a Tony Morris, PhD, b and Peter Gibbons, MB, BS, DO,a
ABSTRACT Background: One of the diagnostic characteristics of the manipulable spinal lesion—a musculoskeletal disturbance
detected by manual palpation and corrected with manipulation—is said to be altered segmental tissue texture. Various manual therapy authors have speculated on the possible nature of this tissue change, with some authors hypothesizing that it represents deep segmental muscle overactivity. Objectives: To review the literature relating to the detection and nature of altered paraspinal tissue texture, proposed explanations for altered tissue texture, evidence for the plausibility of paraspinal muscle spasm, and evidence of muscle dysfunction associated with low back pain (LBP). Data Source: MEDLINE and CINAHL databases were searched using various combinations of the keywords paraspinal, muscle, palpation, EMG, spine, low back pain, pain, myofascial, hardness, manipulation, reliability, and somatic dysfunction, along with searching the bibliographies of selected articles and textbooks. Data Extraction: All relevant data were used. Results: Little direct evidence exists for the nature of abnormal paraspinal tissue texture detected by palpation. Palpation for tenderness is more reliable than palpation for tissue texture change. Indirect evidence from animal studies and experimental muscle inflammation support the plausibility of protective paraspinal muscle contraction. Increased paraspinal electromyographic (EMG) activity observed in subjects with LBP appears to be a result of voluntary and nonvoluntary changes in motor control, modified by psychophysiological responses to perceived stress rather than a simple protective reflex. Conclusion: Although little direct evidence exists of the nature of clinically detected paraspinal tissue texture change, the concept of reactive muscle contraction appears plausible. Increased paraspinal EMG activity associated with LBP does not appear to be mediated by a simple protective reflex. (J Manipulative Physiol Ther 2004;27:267-74) Key Indexing Terms: Spine; Muscle; Palpation; Chiropractic; Osteopathic Medicine
INTRODUCTION
P
alpation of musculoskeletal tissues forms a major part of physical examination for practitioners in many disciplines of manual therapy. For practi-
a School of Health Science, Victoria University, Melbourne, Australia. b Faculty of Human Development, Victoria University, Melbourne, Australia. Submit requests for reprints to: Gary Fryer, School of Health Science, City Campus Victoria University, PO Box 14428 MCMC, Melbourne 8001, Australia (e-mail: [email protected]). Paper submitted December 2, 2002. 0161-4754/$30.00 Copyright n 2004 by National University of Health Sciences. doi:10.1016/j.jmpt.2004.02.006
tioners of osteopathy and chiropractic, paraspinal tissue texture changes are thought to be associated with the manipulable spinal lesion and are proposed by some authors to be a diagnostic indicator—and even a cause—of intervertebral dysfunction.1-3 The nature of deep paraspinal tissue abnormalities detected by palpation, however, has been underresearched and is largely speculative. This is the first of two papers that will review and examine the proposed explanations for deep paraspinal tissue texture change and the evidence supporting these explanations. MEDLINE and CINAHL databases were searched using various combinations of the keywords paraspinal, muscle, palpation, EMG, spinal, low back pain, pain, myofascial, hardness, manipulation, reliability, and somatic dysfunction, along with searching the bibliographies of selected articles and textbooks. 267
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This article will review the practice of palpation to detect altered paraspinal tissue texture, explanations for paraspinal muscle dysfunction, evidence for the rationale of paraspinal muscle spasm, and the evidence for increased paraspinal muscle electromyographic (EMG) activity associated with low back pain (LBP). Part 2 will examine the evidence for decreased paraspinal EMG activity associated with LBP, deep paraspinal muscle atrophy, nonparaspinal muscle dysfunction, the effect of manipulation on paraspinal muscle EMG activity, and how this evidence may relate to tissue texture abnormalities detected with palpation. Finally, it will outline directions for future research that is needed to determine the exact nature of altered paraspinal tissue texture detected with manual palpation.
DISCUSSION The Manipulable Lesion Authors in the field of manual therapy claim that intervertebral dysfunction (known as somatic dysfunction, segmental dysfunction, chiropractic subluxation, joint blockage, or fixation by the various manipulating professions)1,3-8 can be detected by skilled manual palpation.1,3-5 In osteopathy, the diagnostic indicators of segmental dysfunction are said to be segmental asymmetry of bony landmarks, range of motion abnormality (increased, decreased, or a change in quality), tissue texture changes, and tenderness.1-3 Other manipulative professions use similar diagnostic criteria to diagnose manipulable lesions. Physiotherapists place emphasis on the altered quality of joint motion or ‘‘end-feel,’’9-11 whereas the chiropractic profession has traditionally emphasized static asymmetry, sometimes employing radiographic analysis to determine positional asymmetry.6,7
Palpation of Paraspinal Tissue Changes Osteopathic authors have reported that segmental tissue texture changes may include abnormal hardness, bogginess, or ropiness of the underlying paraspinal muscles.1,3,12 Osteopaths commonly palpate for altered tissue texture in 3 distinct paraspinal regions: the medial paraspinal groove or ‘‘gutter,’’ which lies close to the spine between the vertebral spinous process in the midline and the erector spinae muscle group; the bulk of the erector spinae muscle group; and, more laterally, the iliocostalis muscle fibers overlying the angles of the ribs. Many authors claim that the cardinal sign of intervertebral dysfunction is palpable hypertonicity of the deep fourth layer paraspinal muscles, particularly rotatores and multifidus,1,3,12-14 which can be palpated in the medial paraspinal groove.1,3 It is usually found unilaterally and reported as being tender by the patient. More laterally, palpable hypertonicity of the iliocostalis muscle at the rib angle is claimed to be indicative of rib dysfunction.3
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Reliability of Palpation for Tissue Texture Change Although the use of palpation to detect abnormal tissue texture and tenderness is commonplace and used by all manual therapy professions, the reliability and accuracy of palpation to detect muscle dysfunction is not well established in the scientific literature. Of all the diagnostic signs of intervertebral dysfunction – asymmetry of bony landmarks, range of motion abnormality, tissue texture changes, and tenderness – palpation for tenderness appears to be the most reliable.15-18 The reliability of palpation for spinal tenderness has been supported by a number of studies.15-18 Boline et al15 evaluated different approaches to identifying lumbar segmental abnormalities and found palpation for tenderness to be the most reliable, producing good to excellent interexaminer agreement. Boline et al15 found that the reliability of palpation for pain over the lumbar spinous processes was slightly higher (K = .48-.90) than for palpation of lumbar paraspinal soft tissue pain (K = .40-.79). Hubka and Phelan16 reported that palpation of cervical spine tenderness (over the spinous processes) was highly reliable (K = .68). Nilsson17 also found acceptable reliability (r = .88) of palpation for cervical erector spinae muscle tenderness, using a grading pain scale of 0 to 3 that incorporated both verbal and nonverbal responses from the patient. Recently, Christensen et al18 also reported good interexaminer reliability for thoracic paraspinal tenderness. The interexaminer agreement for the detection of tissue texture changes within muscle tissue appears to be less reliable than the detection of tenderness. Investigators who have attempted to establish the reliability of detecting myofascial trigger points (taut bands of skeletal muscle that are tender on palpation and refer characteristic pain)19 have found tenderness to be a reliable feature but report varying results for palpation of the taut band.20-23 Njoo and Van der Does20 noted that palpable bands seem to occur without the presence of localized tenderness or complaint of pain and raise the possibility that muscle texture changes without tenderness may represent normal muscle heterogeneity. A variety of tissue compliance devices have been used to investigate muscle hardness.24-26 Although one device has been demonstrated to detect harder muscles in patients with tension-type headaches than control subjects,27,28 the reliability of these devices remains uncertain. Some researchers have found handheld compliance meters to have good intraexaminer reliability,29,30 good interexaminer reliability,31 and poor interexaminer reliability.26,32 One automated device has been reported to have excellent reliability and accuracy in determining the compliance of foam surfaces,26 but it was subject to problems and variations in human participants.33 Until such devices have been shown to demonstrate high interexaminer reliability and accuracy in determining tissue hardness in human subjects, they cannot be used as a valid measure of manual palpation.
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Proposed Explanations for Altered Tissue Texture Associated with Intervertebral Dysfunction There has been much speculation on the etiology of the manipulable lesion, with various authors implicating the paraspinal muscles, zygapophysial joints, and the intervertebral disk as the underlying cause of motion restriction and tissue texture change. The model most accepted in the field of osteopathy and still quoted in most osteopathic texts3,5,34-36 is Korr’s neurological concept of the facilitated segment, which implicates the deep paraspinal musculature as the prime cause of restricted segmental mobility and tissue texture change. From the 1940s to the early 1960s, osteopathic researchers Denslow et al and Korr et al37-42 conducted studies that they claimed provided evidence of segmental spinal cord hyperactivity, which Denslow first called the ‘‘central excitatory state.’’ They reported evidence of increased segmental muscle activity and segmental sympathetic nervous system output at spinal levels associated with clinically detected segmental dysfunctions. Korr43 developed the ‘‘facilitated segment’’ concept, where he proposed that minor unanticipated trauma could produce a discordant barrage of afferent input into the spinal cord from muscle spindle proprioceptors. This discordant ‘‘noise’’ would enter the dorsal horn of the spinal cord and alter the firing thresholds and excitability of the interconnecting neurons, bringing the normally anonymous segment ‘‘into view’’ of the central nervous system. All activity passing through that segment would become exaggerated, producing increased nociception, a and g motor activity to segmental muscles, and sympathetic output. This model attempted to explain the clinical findings of segmental dysfunction: tenderness and pain due to facilitated ascending nociception, joint range of motion restriction due to the resistance of shortened and overactive muscles, and tissue texture changes due to sustained muscle contraction and sympathetic induced circulatory changes.43 The concepts of ‘‘muscle spasm’’ and ‘‘pain-spasm-pain cycle’’ are popular explanations for hard and tender muscles, but the evidence to support these concepts is lacking.44 Lederman45 has criticized the belief, common in manual therapies, that relaxed muscles normally display a low level of motor contraction (‘‘neurological muscle tone’’) that may be ‘‘turned up’’ when dysfunction occurs. ‘‘Neurological’’ muscle tone appears to be controversial, as some authorities in the field of EMG claim that relaxed muscles have no motor activity,46 whereas others state that low-level motor unit firing contributes to resting muscle tone.47 The assessment of very low-level EMG activity in paraspinal muscles is complicated by the electrical noise generated by the heart, respiratory muscles, and extraneous sources of noise.48 The greatest weakness in all models that attribute muscle spasm as the cause of altered tissue texture and joint motion loss is the lack of evidence of abnormal motor activity associated with these clinical findings. The studies by
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Denslow et al and Korr et al37-42 are over 50 years old and were, by today’s standards, poorly described with insufficient data reported and no statistical analysis. Slosberg49 suggested that the diameter of the needles used by Denslow were larger and more disruptive than the fine-wire needle electrodes used today. Reproduction of these studies with modern equipment would help verify their significance. Hubbard et al50 recently examined the EMG activity of relaxed paraspinal muscles and found no significant differences between those detected as tender and abnormal with palpation and nontender muscles. This pilot study should be regarded as inconclusive due to its small sample size and problems encountered with noise and cardiac artefact. Interestingly, the one symptomatic subject in the study displayed a large increase in EMG activity over the painful site. Even Denslow51 had misgivings about their original research. In 1975, 34 years after the publication of his original article, Denslow conceded that not all palpable paraspinal tissue texture changes could be explained by muscle contraction. He suggested that it was possible that some inflammatory process may account for the abnormal tissues.51 Despite these admissions and the lack of corroborating evidence, Denslow’s work is still commonly cited to support the theory of paraspinal muscle spasm.34-36,52
Evidence for the Rationale for Muscle Spasm Because direct evidence of muscle activity associated with palpable abnormalities is not available, the question of the plausibility of the concept of muscle spasm must be explored. Recent experimental evidence has provided some support for the rationale of paraspinal muscle spasm secondary to injury of elements of the spinal joint complex. In animal experiments, researchers have demonstrated the existence of reflex pathways between a number of deep spinal structures and the paraspinal muscles. In addition, there is some evidence that muscle inflammation alters the stretch sensitivity of the muscle spindle proprioceptor and may produce reflex-mediated muscle stiffness.
Muscle Spasm as a Protective Reflex Indahl et al53 electrically stimulated the annulus fibrosis of the intervertebral disk (IVD) and zygapophysial joint capsule at the L1-2 motion segments of 15 pigs and found that stimulation of the joint capsule produced reflex multifidus activity on the same side and segmental level, whereas unilateral annulus stimulation produced activity on both sides and at different levels. Injections of lidocaine (an anesthetic) into the zygapophysial joint markedly reduced the reflex paraspinal activity. Indahl et al53 concluded that joint capsule sprain could activate the paraspinal musculature and that LBP could be due to a combination of pain from injured structures and long-standing contraction of the multifidus muscles.
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Researchers have demonstrated that electrical stimulation and mechanical deformation of the supraspinous ligament can produce reflex activation of the paraspinal muscles, which are most likely to be protective reflexes to produce unloading of the injured ligament. Stubbs et al54 electrically stimulated the supraspinous ligaments of 6 anesthetized cats and recorded fast and powerful reflex paraspinal muscle contraction. Williams et al55 demonstrated that prolonged flexion of the feline lumbar spine (by placing a load on the supraspinous ligament) produced initial reflex activity of the multifidus, which diminished in 3 minutes, and was followed by random bursts of activity, which Williams et al55 termed ‘‘spasms.’’ Solomonow et al56 examined the effect of mechanical deformation of the supraspinous ligament in 12 cats and reported that strong reflex multifidus activation was produced in the isolated ligament only when the stress in the ligament approached magnitudes causing risk or rupture of the tissue. Solomonow et al56 also electrically stimulated the supraspinous ligaments in 3 patients undergoing spinal surgery and recorded EMG discharges from the paraspinal muscles of 2 patients. Thus, Solomonow et al56 were able to confirm that electrical stimulation and mechanical deformation of the supraspinous ligament can elicit reflex paraspinal muscle activity and that such a reflex exists in humans.
Muscle Spindle Sensitization Johansson and Sojka57 proposed a model that attempted to explain the pathophysiological mechanisms of the origin, spread, and perpetuation of muscle pain and tension in chronic pain syndromes. They suggested that the activity of muscle spindle afferents might be increased due to fusimotor (spindle) reflex effects induced by chemosensitive muscle afferents. These afferents could be excited by chemicals liberated during muscle pain, inflammation, ischemia, and sustained muscle contraction. The activation of these afferents would cause pain and disturb proprioception and motor control via their effects on the g-muscle spindle system. Pederson et al58 argued that increased activity in the fusimotor reflex loop would not increase the resting activity of the a-motor system (resting EMG activity) but would increase the stretch sensitivity of the muscle spindles and increase reflex-mediated muscle stiffness. This hypothesis would mean that there would be no increase in resting EMG activity of the involved muscles but increased activity during active or passive stretching and altered EMG patterns during normal activities. Pedersen et al58 found that bradykinin (a chemical that promotes inflammation) injected into the trapezius and splenius muscles of anesthetized cats produced large and long lasting increases in the static stretch-sensitivity of muscle spindle afferents, supporting the hypothesis of Johansson and Sojka.57 Wang et al59 also demonstrated that experimental muscle pain in the masseter muscle increased
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the stretch reflexes of the jaw muscles of volunteers. Matre et al60 used hypertonic saline infusions to create muscle pain in the tibialis anterior and soleus muscles of 14 human volunteers. Matre et al61 reported an increase in the amplitude of the stretch reflex, suggesting increased muscle spindle sensitivity, but no change in the excitability of the a-motor neurone pool (as evidenced by the H-reflex). The increased stretch reflex appeared to occur only in the relaxed muscle. Increased spindle sensitivity may be less important when the muscle is functionally active, but it may be relevant to the detection of tissue changes due to the slight stretch produced when palpating a relaxed muscle. Although these studies support the theory of chemically induced muscle spindle sensitivity, 2 recent studies have failed to support the proposal of increased spindle sensitivity in LBP.62,63 The evidence for protective reflex muscle contraction and increased muscle spindle sensitivity lends credibility to the theory of muscle contraction as a component of intervertebral dysfunction. Although this theory would seem to have a plausible foundation, what must follow is evidence establishing increased or altered EMG activity of paraspinal muscles in regions detected as tender and abnormal to palpation.
Evidence of Paraspinal Muscle Dysfunction Associated with LBP Over the last 2 decades, there has been considerable effort to establish the etiology of LBP and whether the paraspinal muscles of subjects with LBP are functionally or anatomically different from their healthy counterparts. At first glance, much of this evidence is conflicting and confusing, because some studies have reported increased muscle activity, others have reported decreased activity, and a few studies have reported both. It seems possible to clarify this situation by identifying certain conditions where either increased or decreased paraspinal activity has consistently been demonstrated to explain the mechanisms behind the disturbed function. It is possible that this body of research has relevance to the nature of tender and abnormal paraspinal muscles, because osteopaths and chiropractors see segmental dysfunction as having a role in spinal pain. It would be incorrect, however, to assume that any changes in muscles of subjects with LBP necessarily occur in regions detected with palpation, because many believe that segmental dysfunction can commonly occur in asymptomatic subjects. Furthermore, it is not certain whether the functional and anatomical changes that occur in muscles associated with LBP have a causal role in LBP or are simply a result of adaptation due to modified behavior.
Increased Activity of Paraspinal Muscles Associated with LBP There is evidence for increased EMG activity of the lumbar paraspinal muscles under certain conditions. In many of these circumstances, it is unknown whether the abnormal activity is a cause of LBP or simply a consequence
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or adaptation to it and whether it could be a spinal cord reflex or a more complex change in central nervous system (CNS) control.
Decreased Flexion-Relaxation The most consistent demonstration of increased paraspinal muscle activity in LBP, relative to healthy control subjects, has been the lack of lumbar muscle relaxation when the trunk is fully flexed.63-69 When pain-free subjects perform active full trunk flexion, there is normally minimal activity of the lumbar paraspinal muscle at the end of flexion, presumably as the trunk can be supported in this position by the tension of the posterior spinal ligaments. Many researchers have reported the loss of this flexionrelaxation response63-69 in LBP, as well as a reduced range of flexion63-65,67 and decreased paraspinal EMG activity when reextending.63,64,66,68,69 It is unknown whether the lack of paraspinal muscle relaxation during full trunk flexion is produced by a reflex from injured spinal ligaments, an unconscious guarding action as painful ligaments are stretched, or simply due to apprehension of a patient who believes further flexion will produce more pain and injury. Nouwen et al68 suggested that patients with chronic LBP move differently, possibly flexing from the hips and keeping their backs extended, which would explain the increased paraspinal activity in the flexed position. Ahern et al64,65 noted that the majority of chronic LBP patients failed to achieve the range of flexion where the relaxation response was likely to occur (63j F 13j) and concluded that guarded movement (slow cautious movement and/or decreased velocity relative to baseline; nonmethodical or jerky movement) explained approximately 27% of the variability in the relaxation response. Mannion et al70 reported, however, that there was no significant relationship between changes in the degree of flexion-relaxation and the range of lumbar flexion. Zedka et al63 examined the effect of experimentally induced pain (computer regulated saline infusion into the right lumbar erector spinae muscles) on paraspinal muscle activity. During trunk flexion, pain spontaneously decreased the velocity and range of trunk motion, paraspinal relaxation in maintained flexion was absent, and decreased paraspinal EMG activity occurred on reextension. When subjects were asked to voluntarily overcome this guarding strategy and be guided to perform flexion and extension at a prepain velocity and range, the EMG activity was similar, with only the left nonpainful paraspinal muscles achieving some degree of relaxation. Zedka et al63 questioned the view that the increased muscle activity in full flexion was a protective reflex initiated from the loading of injured spinal ligaments, because in their study the ligaments were uninjured and painless. They argued that the persistence of EMG changes, even when subjects overcame their natural tendency to move more slowly and over a smaller range while in pain,
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suggested a more complex mechanism. They proposed that pain in any lumbar structure (ligament, joint, or muscle) may have produced a change in CNS strategy, which resulted in the muscle working in ‘‘pain mode’’ to protect the spine from extreme movement whenever pain was signalled.63 It is likely that the lack of flexion-relaxation exhibited by subjects with LBP can be due to both voluntary guarding behavior and a change in CNS strategy. Protective reflex contraction initiated from injured ligaments seems unlikely, given that the phenomena occurred with experimentally induced muscle pain alone. The relevance of this increased paraspinal activity to abnormally palpable resting paraspinal muscles is unclear. If a change in CNS strategy as a reaction to spinal pain results in paraspinal muscles working in an overprotective ‘‘pain mode,’’ it may be possible that nonvoluntary muscle guarding also occurs when the muscles are being palpated. This hypothesis has not yet been examined. No study has yet examined whether the resting activity of paraspinal muscles changes during the procedure of palpation.
Increased Activity in Static Postures Increased paraspinal activity in LBP patients has been demonstrated to occur in certain static postures, particularly while standing. Arena et al71 examined patients in different postures who were grouped according to their LBP diagnosis. They found that the combined LBP patient groups, while quietly standing, had significantly higher paraspinal EMG levels than the pain-free control subjects. When the results of all the different positions examined (standing, bending, rising, unsupported sitting, supported sitting) were combined, the IVD disorder and unspecified musculoskeletal backache groups had significantly higher EMG levels than the controls. Interestingly, the mean EMG activity of all LBP groups resting in the prone position was higher than the nonpain controls but did not reach statistical significance. Sihvonen et al69 reported that 74% of subjects with ongoing LBP showed distinct EMG activity with both surface and intramuscular recordings of paraspinal muscles while standing. This contrasted with the healthy subjects whose standing EMG activity was hardly noticeable. Ambroz et al66 found the paraspinal EMG activity of the subjects with LBP (matched for age, sex, and body mass index) in a relaxed standing position was 3 times higher than the healthy controls. It is possible that protective reflex muscle contraction may occur in acute conditions where moderate tissue damage has occurred (such as IVD prolapse with acute scoliosis and loss of lordosis), but this seems unlikely to be the mechanism occurring in most cases of LBP. Increased muscle activity in static positions, particularly standing, may be better explained by a combination of voluntary guarding and an altered CNS strategy that causes muscles to behave in ‘‘pain mode,’’ as suggested by Zedka et al.63 While these
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studies lend support to the proposal of muscle overactivity being associated with LBP and palpable paraspinal abnormalities, there still remains a lack of evidence demonstrating this increased activity in muscles that are detected as tender and abnormal to palpation.
Psychophysiological Response to Pain Flor et al72 have demonstrated that stressful events may trigger very specific muscle hyperactivity patterns in individuals with chronic pain. When volunteers with chronic LBP discussed stressful life events or their pain episodes, they responded with marked increases of EMG activity in their lumbar paraspinal musculature but not when reciting nonstressful tasks such as the alphabet or mental arithmetic. Flor et al72 interpreted this as a symptom-specific muscular response stereotypy to personally relevant stress. In a later study, Flor et al73 recorded EMG responses from subjects with LBP, subjects with temporomandibular pain, and healthy controls and asked them to imagine a stressful event that occurred in the past week or to undertake neutral imagery (sitting at home). Flor et al73 found that there was a significant difference between the subjects with LBP and the controls for left erector spinae activity during the stressful imagery and of masseter activity between the temporomandibular pain patients and controls. The EMG activity was increased at the site of pain but not at distal sites (such as trapezius, biceps, or masseter in the LBP patients). Flor et al73 found there were high variances in the muscles of the LBP subjects, indicating that some responded with very high activity, whereas others showed normal responses. The absolute stress-related EMG changes in microvolts were quite small, but Flor et al73 argued that the stressors were imagined and stressors outside the laboratory may evoke much larger responses. Increased resting muscle activity following mental imagery has also been reported by Stohler et al,74 who compared the effect of experimental jaw muscle pain to the effect of mentally recalling an episode of pain. Both the experimentally produced pain and the imagined pain produced similar significant increases in resting EMG levels of temporalis and masseter muscles. Stohler et al74 noted that the resting EMG increases were very small (0.53-0.70lv in experimental pain and 0.63-0.91lv during imagined pain) relative to maximal contraction and believed that it was excessive to call these muscles ‘‘hyperactive.’’ They doubted the likelihood that such tiny increases would produce further muscle pain. The evidence of symptom-specific psychophysiological responses to stress in chronic pain patients suggests that emotional and psychological mechanisms further modify the CNS strategy in reaction to pain. Although Stohler et al74 questioned the relevance of such small increases in resting muscle activity, it is feasible that this increase in activity may make the muscle feel different to palpation. Furthermore, it seems likely that exposure to chronic pain or recurrent
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episodes of acute pain may produce a stronger stereotypical, psychophysiological response in susceptible individuals. It seems possible that most reports of increased paraspinal EMG activity in LBP patients may be explained as a combination of voluntary guarding behavior65,68 and a change in CNS strategy, producing exaggerated ‘‘pain mode’’ muscle activity to limit excessive or unanticipated movement.63 Emotional and psychological experience of chronic pain may further modify or reinforce this altered CNS strategy to produce stereotypical patterns of guarding activity in response to real or imagined stress. The relevance of this abnormally increased muscle activity to paraspinal regions that are tender and feel abnormal to palpation remains untested, but it is feasible that increased muscle activity may be detectible with palpation and even the act of palpation may provoke further muscle guarding.
CONCLUSION Although there is little direct evidence to support the belief that sustained muscle contraction is a feature of intervertebral dysfunction, the concept of protective muscle spasm appears plausible. Reflex multifidus muscle contraction has been demonstrated following electrical and mechanical stimulation of deep spinal structures in animals, and such a reflex has been demonstrated to exist in humans. Additionally, experimental muscle inflammation has been demonstrated to produce increased fusimotor activity and reflex-mediated muscle stiffness. Increased paraspinal muscle activity has been observed in LBP patients during full flexion, static postures, and as a reaction to stressful imagery. It appears that while voluntary guarding behavior may be responsible for increased activity in some patients, increased muscle activity is, in part, due to a nonvoluntary change in CNS control, a proposed ‘‘pain mode’’ strategy in response to pain originating from any spinal structure. There is evidence to support the proposal of abnormally increased paraspinal muscle activity as a consequence of spinal injury. Similar changes to those found in LBP patients may occur in the muscles adjacent to intervertebral injury and produce the commonly reported clinical findings of tenderness and altered tissue texture at a single intervertebral level. What must follow, however, is direct evidence of increased EMG activity associated with the detection of tender and abnormal to palpation paraspinal regions.
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pelvis. An osteopathic perspective. London: Churchill Livingstone; 2000. p. 5-6. Greenman PE. Principles of manual medicine. 2nd ed. Baltimore: William & Wilkins; 1996. p. 1-30. Kappler RE. Palpatory skills. In: Ward RC, editor. Foundations for osteopathic medicine. Baltimore: Williams & Wilkins; 1997. p. 473-7. DiGiovanna EL, Schiowitz S. An osteopathic approach to diagnosis and treatment. 2nd ed. Lippincott; 1997. p. 6-12. Gatterman MI. Foundations of chiropractic: subluxation. St. Louis: Mosby; 1995. p. 176-89. Leach RA. The chiropractic theories: principles and clinical applications. 3rd ed. Baltimore: William & Wilkins; 1994. p. 23-39. Grieve GP. Common vertebral joint problems. Edinburgh: Churchill-Livingstone; 1981. Jull GA, Bogduk N, Marsland A. The accuracy of manual diagnosis for cervical zygapophysial joint pain syndromes. Med J Aust 1988;148:233-6. Jull GA, Treleaven J, Versace G. Manual examination: is pain provocation a major cue for spinal dysfunction? Australian J Physiother 1994;40:159-65. Corrigan B, Maitland GD. Practical orthopaedic medicine. Cambridge, England: Butterworth & Co; 1983. p. 12-15. Walton WJ. Textbook of osteopathic diagnosis and technique procedures. Ohio: American Academy of Osteopathy; 1970. p. 160-1. Bourdillon JF. Spinal manipulation. 5th ed. London: Butterworth-Heinemann; 1992. p. 298. Stoddard A. Manual of osteopathic techniques. 3rd ed. London: Hutchinson & Co.; 1980. p. 25-36. Boline PD, Haas M, Meyer JJ, Kassek K, Nelson C, Keating JC. Interexaminer reliability of eight evaluative dimensions of lumbar segmental abnormality: part 2. J Manipulative Physiol Ther 1993;16:363-74. Hubka MJ, Phelan SP. Interexaminer reliability of palpation for cervical spine tenderness. J Manipulative Physiol Ther 1994;17:591-4. Nilsson N. Measuring cervical tenderness. J Manipulative Physiol Ther 1995;18:88-90. Christensen HW, Vach W, Vach K, Manniche C, Haghfelt T, Hartvigsen J, et al. Palpation of the upper thoracic spine: an observer reliability study. J Manipulative Physiol Ther 2002; 25:285-92. Travell JG, Simons DG. Myofascial pain and dysfunction. 1st ed. Baltimore: William & Wilkins; 1983. p. 5-44. Njoo KH, Van der Does E. The occurrence and inter-rater reliability of myofascial trigger points in the quadratus lumborum and gluteus medius: a prospective study in non-specific low back pain patients and controls in general practice. Pain 1994;58:317-23. Nice DA, Riddle DL, Lamb RL, Mayhew TP, Rucker K. Intertester reliability of judgements of the presence of trigger points in patients with low back pain. Arch Phys Med Rehabil 1992;73:893-8. Tunks E, McCain GA, Hart LE, Teasell RW, Goldsmith CH, Rollman GB, et al. The reliability of examination for tenderness in patients with myofascial pain, chronic fibromyalgia and controls. J Rheumatol 1995;22:944-52. Gerwin R, Shannon S, Hong C, Hubbard D, Gervirtz R. Interrater reliability in myofascial trigger point examination. Pain 1997;69:65-73. Fischer AA. Tissue compliance meter for objective, quantitative documentation of soft tissue consistency and pathology. Arch Phys Med Rehabil 1987;68:122-5.
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25. Horikawa M, Ebihara S, Sakai F, Akiyama M. Non-invasive measurement method for hardness in muscular tissues. Med Biol Eng Comput 1993;31:623-7. 26. Kawchuk GK, Herzog W. A new technique of tissue stiffness (compliance) assessment: its reliability, accuracy and comparison with an existing method. J Manipulative Physiol Ther 1996;19:13-8. 27. Saikai F, Ebihara S, Akiyama M, Horikawa M. Pericranial muscle hardness in tension-type headache. A non-invasive measurement method and its clinical application. Brain 1995; 118:523-31. 28. Ashina M, Bendtsen L, Jensen R, Sakai F, Olesen J. Muscle hardness in patients with chronic tension-type headache: relation to actual headache state. Pain 1999;79:201-5. 29. Sanders GE, Lawson DA. Stability of paraspinal tissue compliance in normal subjects. J Manipulative Physiol Ther 1992; 15:361-4. 30. Ashina M, Bendtsen L, Jensen R, Sakai F, Olesen J. Measurement of muscle hardness: a methodological study. Cephalalgia 1998;18:106-11. 31. Waldorf T, Devlin L, Nansel D. The comparative assessment of paraspinal tissue compliance in asymptomatic female and male subjects in both prone and standing positions. J Manipulative Physiol Ther 1991;14:457-61. 32. Kawchuk GK, Herzog W. The reliability and accuracy of a standard method of tissue compliance assessment. J Manipulative Physiol Ther 1995;18:298-301. 33. Kawchuk GK, Fauvel OR. Sources of variation in spinal indentation testing: indentation site relocation, intraabdominal pressure, subject movement, muscular response, and stiffness estimation. J Manipulative Physiol Ther 2001;24:84-91. 34. Chaitow L. Muscle energy techniques. Edinburgh: Churchill Livingstone; 1996. p. 18-20. 35. Kuchera WA, Kuchera ML. Osteopathic principles in practice. Missouri: Kirksville College of Osteopathic Medicine Press; 1992. p. 33-5, 71-5. 36. Mitchell FLJ. The muscle energy manual. Vol 1. Michigan: MET Press; 1995. p. 25-33. 37. Denslow JS, Clough GH. Reflex activity in the spinal extensors. J Neurophysiol 1941;4:430-7. 38. Denslow JS, Korr IM, Krems AD. Quantitative studies of chronic facilitation in human motorneuron pools. 1947;150(2). 39. Denslow JS. An analysis of the variability of spinal reflex thresholds. J Neurophysiol 1944;7:207-13. 40. Denslow JS, Hassett CC. The central excitatory state associated with postural abnormalities. J Neurophysiol 1942;5:393-402. 41. Korr IM, Wright HM, Thomas PE. Effects of experimental myofascial insults on cutaneous patterns of sympathetic activity in man. J Neural Transm 1962;23:330-55. 42. Korr IM, Thomas PE, Wright HM. Patterns of electrical skin resistance in man. J Neural Transm 1958;17:77-96. 43. Korr IM. The neural basis of the osteopathic lesion. J Am Osteopath Assoc 1947;47:191-8. 44. Roland MO. A critical review of the evidence for a painspasm-pain cycle in spinal disorders. Clin Biomech (Bristol, Avon) 1986;1:102-9. 45. Lederman E. Fundamentals of manual therapy. London: Churchill Livingstone; 1947. p. 133-7. 46. Basmajian JV, De Luca CJ. Muscles alive: their function revealed by electromyography. 5th ed. Baltimore: William & Wilkins; 1985. 47. Guyton AC, Hall JE. Textbook of medical physiology. 10th ed. Philadelphia: WB Saunders Co; 2000. p. 76. 48. Cram JR, Kasman GS. Introduction to surface electromyography. Gaithersburg (MD): Aspen; 1998. p. 67-9.
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49. Slosberg M. Effects of altered afferent articular input on sensation, proprioception, muscle tone and sympathetic reflex responses. J Manipulative Physiol Ther 1988;11:400-8. 50. Hubbard A, Fryer G, McLaughlin P. An investigation into the electrical activity of tender, resting paraspinal muscles using surface electromyography: a pilot study. J Osteopath Med 2002;5:59-64. 51. Denslow JS, Denslow JS. Pathophysiological evidence for the osteopathic lesion: the known, unknown and controversial. J Am Osteopath Assoc 1975;75:415-21. 52. Stone C. Science in the art of osteopathy. UK: Stanley Thornes Ltd; 1999. p. 75-7. 53. Indahl A, Kaigle A, Reikeras O, Holm S. Electromyographic response of the porcine multifidus musculature after nerve stimulation. Spine 1995;20:2652-8. 54. Stubbs M, Harris M, Solomonow M, Zhou B, Lu R, Baratta V. Ligamento-muscular protective reflex in the lumbar spine of the feline. J Electromyogr Kinesiol 1998;8:197-204. 55. Williams M, Solomonow M, Zhou B, Baratta V, Harris M. Multifidus spasms elicited by prolonged lumbar flexion. Spine 2000;25:2916-24. 56. Solomonow M, Zhou B, Harris M, Lu R, Baratta V. The ligamento-muscular stabilizing system of the spine. Spine 1998;23:2552-62. 57. Johansson H, Sokja P. Pathophysiological mechanisms involved in genesis and spread of muscle tension in occupational muscle pain and in chronic musculoskeletal pain syndromes. A hypothesis. Med Hypotheses 1991;35:49-57. 58. Pedersen J, Sjolander P, Wenngren BI, Johansson H. Increased intramuscular concentration of bradykinin increases the static fusimotor drive to muscle spindles in neck muscles of the cat. Pain 1997;70:83-91. 59. Wang K, Svensson P, Arendt-Nielson L. Effect of tonic muscle pain on short-latency jaw-stretch reflexes in humans. Pain 2000;88:189-97. 60. Matre DA, Sinkjaer T, Svensson P, Arendt-Nielson L. Experimental muscle pain increases the human stretch reflex. Pain 1998;75:331-9. 61. Matre DA, Sinkjaer T, Knardahl S, Anderson JB, ArendtNielson L. The influence of experimental muscle pain on the human soleus stretch reflex during sitting and walking. Clin Neurophysiol 1999;110:2033-43.
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62. Kang Y, Wheeler JD, Pickar JG. Stimulation of chemosensitive afferents from multifidus muscle does not sensitize multifidus muscle spindles to vertebral loads in the lumbar spine of the cat. Spine 2001;26:1528-36. 63. Zedka M, Prochazka A, Knight B, Gillard D, Gauthier M. Voluntary and reflex control of human back muscles during induced pain. J Physiol 1999;520:591-604. 64. Ahern DK, Follick MJ, Council JR, Laser-Wolston N, Litchman H. Comparison of lumbar paravertebral EMG patterns in chronic low back pain patients and non-patient controls. Pain 1988;34:153-60. 65. Ahern DK, Hannon DJ, Goreczny AJ, Follick MJ, Parziale JR. Correlation of chronic low-back pain behaviour and muscle function examination of the flexion-relaxation response. Spine 1990;15:92-5. 66. Ambroz C, Scott A, Ambroz A, Talbott EO. Chronic low back pain assessment using surface electromygraphy. J Occup Environ Med 2000;42:660-9. 67. Kaigle A, Wessberg P, Hansson TH. Muscular and kinematic behavour of the lumbar spine during flexion-extension. J Spinal Disord 1998;11:163-74. 68. Nouwen A, Van Akkerveeken PF, Versloot JM. Patterns of muscular activity during movement in patients with chronic low back pain. Spine 1987;12:777-82. 69. Sihvonen T, Partanen J, Hanninen O, Soimakallio S. Electric behaviour of low back muscles during lumbar pelvic rhythum in low back pain patients and healthy controls. Arch Phys Med Rehabil 1991;72:1080-7. 70. Mannion AF, Taimela S, Muntener M, Dvorak J. Active therapy for chronic low back pain. Part 1. Effects on back muscle activation, fatigability, and strength. Spine 2001;26:897-908. 71. Arena J, Sherman RA, Bruno GM, Young TR. Electromyographic recordings of 5 types of low back pain subjects and non-pain controls in different positions. Pain 1989;37:57-65. 72. Flor H, Turk DC, Birbaumer N. Assessment of stress-related psychophysiological reactions in chronic low back pain patients. J Consult Clin Psychol 1985;53:354-64. 73. Flor H, Birbaumer N, Schugens MM, Lutzenberger W. Symptom-specific psychophysiological responses in chronic pain patients. Psychophysiology 1992;29:452-60. 74. Stohler CS, Zhang X, Lund JP. The effect of experimental jaw muscle pain on postural muscle activity. Pain 1996;66:215-21.
ABSTRACT Background: One of the diagnostic characteristics of the manipulable spinal lesion—a musculoskeletal disturbance
detected by manual palpation and corrected with manipulation—is said to be altered segmental tissue texture. Various manual therapy authors have speculated on the possible nature of this tissue change, with some authors hypothesizing that it represents deep segmental muscle overactivity. Objectives: To review the literature relating to the detection and nature of altered paraspinal tissue texture, proposed explanations for altered tissue texture, evidence for the plausibility of paraspinal muscle spasm, and evidence of muscle dysfunction associated with low back pain (LBP). Data Source: MEDLINE and CINAHL databases were searched using various combinations of the keywords paraspinal, muscle, palpation, EMG, spine, low back pain, pain, myofascial, hardness, manipulation, reliability, and somatic dysfunction, along with searching the bibliographies of selected articles and textbooks. Data Extraction: All relevant data were used. Results: Little direct evidence exists for the nature of abnormal paraspinal tissue texture detected by palpation. Palpation for tenderness is more reliable than palpation for tissue texture change. Indirect evidence from animal studies and experimental muscle inflammation support the plausibility of protective paraspinal muscle contraction. Increased paraspinal electromyographic (EMG) activity observed in subjects with LBP appears to be a result of voluntary and nonvoluntary changes in motor control, modified by psychophysiological responses to perceived stress rather than a simple protective reflex. Conclusion: Although little direct evidence exists of the nature of clinically detected paraspinal tissue texture change, the concept of reactive muscle contraction appears plausible. Increased paraspinal EMG activity associated with LBP does not appear to be mediated by a simple protective reflex. (J Manipulative Physiol Ther 2004;27:267-74) Key Indexing Terms: Spine; Muscle; Palpation; Chiropractic; Osteopathic Medicine
INTRODUCTION
P
alpation of musculoskeletal tissues forms a major part of physical examination for practitioners in many disciplines of manual therapy. For practi-
a School of Health Science, Victoria University, Melbourne, Australia. b Faculty of Human Development, Victoria University, Melbourne, Australia. Submit requests for reprints to: Gary Fryer, School of Health Science, City Campus Victoria University, PO Box 14428 MCMC, Melbourne 8001, Australia (e-mail: [email protected]). Paper submitted December 2, 2002. 0161-4754/$30.00 Copyright n 2004 by National University of Health Sciences. doi:10.1016/j.jmpt.2004.02.006
tioners of osteopathy and chiropractic, paraspinal tissue texture changes are thought to be associated with the manipulable spinal lesion and are proposed by some authors to be a diagnostic indicator—and even a cause—of intervertebral dysfunction.1-3 The nature of deep paraspinal tissue abnormalities detected by palpation, however, has been underresearched and is largely speculative. This is the first of two papers that will review and examine the proposed explanations for deep paraspinal tissue texture change and the evidence supporting these explanations. MEDLINE and CINAHL databases were searched using various combinations of the keywords paraspinal, muscle, palpation, EMG, spinal, low back pain, pain, myofascial, hardness, manipulation, reliability, and somatic dysfunction, along with searching the bibliographies of selected articles and textbooks. 267
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This article will review the practice of palpation to detect altered paraspinal tissue texture, explanations for paraspinal muscle dysfunction, evidence for the rationale of paraspinal muscle spasm, and the evidence for increased paraspinal muscle electromyographic (EMG) activity associated with low back pain (LBP). Part 2 will examine the evidence for decreased paraspinal EMG activity associated with LBP, deep paraspinal muscle atrophy, nonparaspinal muscle dysfunction, the effect of manipulation on paraspinal muscle EMG activity, and how this evidence may relate to tissue texture abnormalities detected with palpation. Finally, it will outline directions for future research that is needed to determine the exact nature of altered paraspinal tissue texture detected with manual palpation.
DISCUSSION The Manipulable Lesion Authors in the field of manual therapy claim that intervertebral dysfunction (known as somatic dysfunction, segmental dysfunction, chiropractic subluxation, joint blockage, or fixation by the various manipulating professions)1,3-8 can be detected by skilled manual palpation.1,3-5 In osteopathy, the diagnostic indicators of segmental dysfunction are said to be segmental asymmetry of bony landmarks, range of motion abnormality (increased, decreased, or a change in quality), tissue texture changes, and tenderness.1-3 Other manipulative professions use similar diagnostic criteria to diagnose manipulable lesions. Physiotherapists place emphasis on the altered quality of joint motion or ‘‘end-feel,’’9-11 whereas the chiropractic profession has traditionally emphasized static asymmetry, sometimes employing radiographic analysis to determine positional asymmetry.6,7
Palpation of Paraspinal Tissue Changes Osteopathic authors have reported that segmental tissue texture changes may include abnormal hardness, bogginess, or ropiness of the underlying paraspinal muscles.1,3,12 Osteopaths commonly palpate for altered tissue texture in 3 distinct paraspinal regions: the medial paraspinal groove or ‘‘gutter,’’ which lies close to the spine between the vertebral spinous process in the midline and the erector spinae muscle group; the bulk of the erector spinae muscle group; and, more laterally, the iliocostalis muscle fibers overlying the angles of the ribs. Many authors claim that the cardinal sign of intervertebral dysfunction is palpable hypertonicity of the deep fourth layer paraspinal muscles, particularly rotatores and multifidus,1,3,12-14 which can be palpated in the medial paraspinal groove.1,3 It is usually found unilaterally and reported as being tender by the patient. More laterally, palpable hypertonicity of the iliocostalis muscle at the rib angle is claimed to be indicative of rib dysfunction.3
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Reliability of Palpation for Tissue Texture Change Although the use of palpation to detect abnormal tissue texture and tenderness is commonplace and used by all manual therapy professions, the reliability and accuracy of palpation to detect muscle dysfunction is not well established in the scientific literature. Of all the diagnostic signs of intervertebral dysfunction – asymmetry of bony landmarks, range of motion abnormality, tissue texture changes, and tenderness – palpation for tenderness appears to be the most reliable.15-18 The reliability of palpation for spinal tenderness has been supported by a number of studies.15-18 Boline et al15 evaluated different approaches to identifying lumbar segmental abnormalities and found palpation for tenderness to be the most reliable, producing good to excellent interexaminer agreement. Boline et al15 found that the reliability of palpation for pain over the lumbar spinous processes was slightly higher (K = .48-.90) than for palpation of lumbar paraspinal soft tissue pain (K = .40-.79). Hubka and Phelan16 reported that palpation of cervical spine tenderness (over the spinous processes) was highly reliable (K = .68). Nilsson17 also found acceptable reliability (r = .88) of palpation for cervical erector spinae muscle tenderness, using a grading pain scale of 0 to 3 that incorporated both verbal and nonverbal responses from the patient. Recently, Christensen et al18 also reported good interexaminer reliability for thoracic paraspinal tenderness. The interexaminer agreement for the detection of tissue texture changes within muscle tissue appears to be less reliable than the detection of tenderness. Investigators who have attempted to establish the reliability of detecting myofascial trigger points (taut bands of skeletal muscle that are tender on palpation and refer characteristic pain)19 have found tenderness to be a reliable feature but report varying results for palpation of the taut band.20-23 Njoo and Van der Does20 noted that palpable bands seem to occur without the presence of localized tenderness or complaint of pain and raise the possibility that muscle texture changes without tenderness may represent normal muscle heterogeneity. A variety of tissue compliance devices have been used to investigate muscle hardness.24-26 Although one device has been demonstrated to detect harder muscles in patients with tension-type headaches than control subjects,27,28 the reliability of these devices remains uncertain. Some researchers have found handheld compliance meters to have good intraexaminer reliability,29,30 good interexaminer reliability,31 and poor interexaminer reliability.26,32 One automated device has been reported to have excellent reliability and accuracy in determining the compliance of foam surfaces,26 but it was subject to problems and variations in human participants.33 Until such devices have been shown to demonstrate high interexaminer reliability and accuracy in determining tissue hardness in human subjects, they cannot be used as a valid measure of manual palpation.
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Proposed Explanations for Altered Tissue Texture Associated with Intervertebral Dysfunction There has been much speculation on the etiology of the manipulable lesion, with various authors implicating the paraspinal muscles, zygapophysial joints, and the intervertebral disk as the underlying cause of motion restriction and tissue texture change. The model most accepted in the field of osteopathy and still quoted in most osteopathic texts3,5,34-36 is Korr’s neurological concept of the facilitated segment, which implicates the deep paraspinal musculature as the prime cause of restricted segmental mobility and tissue texture change. From the 1940s to the early 1960s, osteopathic researchers Denslow et al and Korr et al37-42 conducted studies that they claimed provided evidence of segmental spinal cord hyperactivity, which Denslow first called the ‘‘central excitatory state.’’ They reported evidence of increased segmental muscle activity and segmental sympathetic nervous system output at spinal levels associated with clinically detected segmental dysfunctions. Korr43 developed the ‘‘facilitated segment’’ concept, where he proposed that minor unanticipated trauma could produce a discordant barrage of afferent input into the spinal cord from muscle spindle proprioceptors. This discordant ‘‘noise’’ would enter the dorsal horn of the spinal cord and alter the firing thresholds and excitability of the interconnecting neurons, bringing the normally anonymous segment ‘‘into view’’ of the central nervous system. All activity passing through that segment would become exaggerated, producing increased nociception, a and g motor activity to segmental muscles, and sympathetic output. This model attempted to explain the clinical findings of segmental dysfunction: tenderness and pain due to facilitated ascending nociception, joint range of motion restriction due to the resistance of shortened and overactive muscles, and tissue texture changes due to sustained muscle contraction and sympathetic induced circulatory changes.43 The concepts of ‘‘muscle spasm’’ and ‘‘pain-spasm-pain cycle’’ are popular explanations for hard and tender muscles, but the evidence to support these concepts is lacking.44 Lederman45 has criticized the belief, common in manual therapies, that relaxed muscles normally display a low level of motor contraction (‘‘neurological muscle tone’’) that may be ‘‘turned up’’ when dysfunction occurs. ‘‘Neurological’’ muscle tone appears to be controversial, as some authorities in the field of EMG claim that relaxed muscles have no motor activity,46 whereas others state that low-level motor unit firing contributes to resting muscle tone.47 The assessment of very low-level EMG activity in paraspinal muscles is complicated by the electrical noise generated by the heart, respiratory muscles, and extraneous sources of noise.48 The greatest weakness in all models that attribute muscle spasm as the cause of altered tissue texture and joint motion loss is the lack of evidence of abnormal motor activity associated with these clinical findings. The studies by
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Denslow et al and Korr et al37-42 are over 50 years old and were, by today’s standards, poorly described with insufficient data reported and no statistical analysis. Slosberg49 suggested that the diameter of the needles used by Denslow were larger and more disruptive than the fine-wire needle electrodes used today. Reproduction of these studies with modern equipment would help verify their significance. Hubbard et al50 recently examined the EMG activity of relaxed paraspinal muscles and found no significant differences between those detected as tender and abnormal with palpation and nontender muscles. This pilot study should be regarded as inconclusive due to its small sample size and problems encountered with noise and cardiac artefact. Interestingly, the one symptomatic subject in the study displayed a large increase in EMG activity over the painful site. Even Denslow51 had misgivings about their original research. In 1975, 34 years after the publication of his original article, Denslow conceded that not all palpable paraspinal tissue texture changes could be explained by muscle contraction. He suggested that it was possible that some inflammatory process may account for the abnormal tissues.51 Despite these admissions and the lack of corroborating evidence, Denslow’s work is still commonly cited to support the theory of paraspinal muscle spasm.34-36,52
Evidence for the Rationale for Muscle Spasm Because direct evidence of muscle activity associated with palpable abnormalities is not available, the question of the plausibility of the concept of muscle spasm must be explored. Recent experimental evidence has provided some support for the rationale of paraspinal muscle spasm secondary to injury of elements of the spinal joint complex. In animal experiments, researchers have demonstrated the existence of reflex pathways between a number of deep spinal structures and the paraspinal muscles. In addition, there is some evidence that muscle inflammation alters the stretch sensitivity of the muscle spindle proprioceptor and may produce reflex-mediated muscle stiffness.
Muscle Spasm as a Protective Reflex Indahl et al53 electrically stimulated the annulus fibrosis of the intervertebral disk (IVD) and zygapophysial joint capsule at the L1-2 motion segments of 15 pigs and found that stimulation of the joint capsule produced reflex multifidus activity on the same side and segmental level, whereas unilateral annulus stimulation produced activity on both sides and at different levels. Injections of lidocaine (an anesthetic) into the zygapophysial joint markedly reduced the reflex paraspinal activity. Indahl et al53 concluded that joint capsule sprain could activate the paraspinal musculature and that LBP could be due to a combination of pain from injured structures and long-standing contraction of the multifidus muscles.
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Researchers have demonstrated that electrical stimulation and mechanical deformation of the supraspinous ligament can produce reflex activation of the paraspinal muscles, which are most likely to be protective reflexes to produce unloading of the injured ligament. Stubbs et al54 electrically stimulated the supraspinous ligaments of 6 anesthetized cats and recorded fast and powerful reflex paraspinal muscle contraction. Williams et al55 demonstrated that prolonged flexion of the feline lumbar spine (by placing a load on the supraspinous ligament) produced initial reflex activity of the multifidus, which diminished in 3 minutes, and was followed by random bursts of activity, which Williams et al55 termed ‘‘spasms.’’ Solomonow et al56 examined the effect of mechanical deformation of the supraspinous ligament in 12 cats and reported that strong reflex multifidus activation was produced in the isolated ligament only when the stress in the ligament approached magnitudes causing risk or rupture of the tissue. Solomonow et al56 also electrically stimulated the supraspinous ligaments in 3 patients undergoing spinal surgery and recorded EMG discharges from the paraspinal muscles of 2 patients. Thus, Solomonow et al56 were able to confirm that electrical stimulation and mechanical deformation of the supraspinous ligament can elicit reflex paraspinal muscle activity and that such a reflex exists in humans.
Muscle Spindle Sensitization Johansson and Sojka57 proposed a model that attempted to explain the pathophysiological mechanisms of the origin, spread, and perpetuation of muscle pain and tension in chronic pain syndromes. They suggested that the activity of muscle spindle afferents might be increased due to fusimotor (spindle) reflex effects induced by chemosensitive muscle afferents. These afferents could be excited by chemicals liberated during muscle pain, inflammation, ischemia, and sustained muscle contraction. The activation of these afferents would cause pain and disturb proprioception and motor control via their effects on the g-muscle spindle system. Pederson et al58 argued that increased activity in the fusimotor reflex loop would not increase the resting activity of the a-motor system (resting EMG activity) but would increase the stretch sensitivity of the muscle spindles and increase reflex-mediated muscle stiffness. This hypothesis would mean that there would be no increase in resting EMG activity of the involved muscles but increased activity during active or passive stretching and altered EMG patterns during normal activities. Pedersen et al58 found that bradykinin (a chemical that promotes inflammation) injected into the trapezius and splenius muscles of anesthetized cats produced large and long lasting increases in the static stretch-sensitivity of muscle spindle afferents, supporting the hypothesis of Johansson and Sojka.57 Wang et al59 also demonstrated that experimental muscle pain in the masseter muscle increased
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the stretch reflexes of the jaw muscles of volunteers. Matre et al60 used hypertonic saline infusions to create muscle pain in the tibialis anterior and soleus muscles of 14 human volunteers. Matre et al61 reported an increase in the amplitude of the stretch reflex, suggesting increased muscle spindle sensitivity, but no change in the excitability of the a-motor neurone pool (as evidenced by the H-reflex). The increased stretch reflex appeared to occur only in the relaxed muscle. Increased spindle sensitivity may be less important when the muscle is functionally active, but it may be relevant to the detection of tissue changes due to the slight stretch produced when palpating a relaxed muscle. Although these studies support the theory of chemically induced muscle spindle sensitivity, 2 recent studies have failed to support the proposal of increased spindle sensitivity in LBP.62,63 The evidence for protective reflex muscle contraction and increased muscle spindle sensitivity lends credibility to the theory of muscle contraction as a component of intervertebral dysfunction. Although this theory would seem to have a plausible foundation, what must follow is evidence establishing increased or altered EMG activity of paraspinal muscles in regions detected as tender and abnormal to palpation.
Evidence of Paraspinal Muscle Dysfunction Associated with LBP Over the last 2 decades, there has been considerable effort to establish the etiology of LBP and whether the paraspinal muscles of subjects with LBP are functionally or anatomically different from their healthy counterparts. At first glance, much of this evidence is conflicting and confusing, because some studies have reported increased muscle activity, others have reported decreased activity, and a few studies have reported both. It seems possible to clarify this situation by identifying certain conditions where either increased or decreased paraspinal activity has consistently been demonstrated to explain the mechanisms behind the disturbed function. It is possible that this body of research has relevance to the nature of tender and abnormal paraspinal muscles, because osteopaths and chiropractors see segmental dysfunction as having a role in spinal pain. It would be incorrect, however, to assume that any changes in muscles of subjects with LBP necessarily occur in regions detected with palpation, because many believe that segmental dysfunction can commonly occur in asymptomatic subjects. Furthermore, it is not certain whether the functional and anatomical changes that occur in muscles associated with LBP have a causal role in LBP or are simply a result of adaptation due to modified behavior.
Increased Activity of Paraspinal Muscles Associated with LBP There is evidence for increased EMG activity of the lumbar paraspinal muscles under certain conditions. In many of these circumstances, it is unknown whether the abnormal activity is a cause of LBP or simply a consequence
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or adaptation to it and whether it could be a spinal cord reflex or a more complex change in central nervous system (CNS) control.
Decreased Flexion-Relaxation The most consistent demonstration of increased paraspinal muscle activity in LBP, relative to healthy control subjects, has been the lack of lumbar muscle relaxation when the trunk is fully flexed.63-69 When pain-free subjects perform active full trunk flexion, there is normally minimal activity of the lumbar paraspinal muscle at the end of flexion, presumably as the trunk can be supported in this position by the tension of the posterior spinal ligaments. Many researchers have reported the loss of this flexionrelaxation response63-69 in LBP, as well as a reduced range of flexion63-65,67 and decreased paraspinal EMG activity when reextending.63,64,66,68,69 It is unknown whether the lack of paraspinal muscle relaxation during full trunk flexion is produced by a reflex from injured spinal ligaments, an unconscious guarding action as painful ligaments are stretched, or simply due to apprehension of a patient who believes further flexion will produce more pain and injury. Nouwen et al68 suggested that patients with chronic LBP move differently, possibly flexing from the hips and keeping their backs extended, which would explain the increased paraspinal activity in the flexed position. Ahern et al64,65 noted that the majority of chronic LBP patients failed to achieve the range of flexion where the relaxation response was likely to occur (63j F 13j) and concluded that guarded movement (slow cautious movement and/or decreased velocity relative to baseline; nonmethodical or jerky movement) explained approximately 27% of the variability in the relaxation response. Mannion et al70 reported, however, that there was no significant relationship between changes in the degree of flexion-relaxation and the range of lumbar flexion. Zedka et al63 examined the effect of experimentally induced pain (computer regulated saline infusion into the right lumbar erector spinae muscles) on paraspinal muscle activity. During trunk flexion, pain spontaneously decreased the velocity and range of trunk motion, paraspinal relaxation in maintained flexion was absent, and decreased paraspinal EMG activity occurred on reextension. When subjects were asked to voluntarily overcome this guarding strategy and be guided to perform flexion and extension at a prepain velocity and range, the EMG activity was similar, with only the left nonpainful paraspinal muscles achieving some degree of relaxation. Zedka et al63 questioned the view that the increased muscle activity in full flexion was a protective reflex initiated from the loading of injured spinal ligaments, because in their study the ligaments were uninjured and painless. They argued that the persistence of EMG changes, even when subjects overcame their natural tendency to move more slowly and over a smaller range while in pain,
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suggested a more complex mechanism. They proposed that pain in any lumbar structure (ligament, joint, or muscle) may have produced a change in CNS strategy, which resulted in the muscle working in ‘‘pain mode’’ to protect the spine from extreme movement whenever pain was signalled.63 It is likely that the lack of flexion-relaxation exhibited by subjects with LBP can be due to both voluntary guarding behavior and a change in CNS strategy. Protective reflex contraction initiated from injured ligaments seems unlikely, given that the phenomena occurred with experimentally induced muscle pain alone. The relevance of this increased paraspinal activity to abnormally palpable resting paraspinal muscles is unclear. If a change in CNS strategy as a reaction to spinal pain results in paraspinal muscles working in an overprotective ‘‘pain mode,’’ it may be possible that nonvoluntary muscle guarding also occurs when the muscles are being palpated. This hypothesis has not yet been examined. No study has yet examined whether the resting activity of paraspinal muscles changes during the procedure of palpation.
Increased Activity in Static Postures Increased paraspinal activity in LBP patients has been demonstrated to occur in certain static postures, particularly while standing. Arena et al71 examined patients in different postures who were grouped according to their LBP diagnosis. They found that the combined LBP patient groups, while quietly standing, had significantly higher paraspinal EMG levels than the pain-free control subjects. When the results of all the different positions examined (standing, bending, rising, unsupported sitting, supported sitting) were combined, the IVD disorder and unspecified musculoskeletal backache groups had significantly higher EMG levels than the controls. Interestingly, the mean EMG activity of all LBP groups resting in the prone position was higher than the nonpain controls but did not reach statistical significance. Sihvonen et al69 reported that 74% of subjects with ongoing LBP showed distinct EMG activity with both surface and intramuscular recordings of paraspinal muscles while standing. This contrasted with the healthy subjects whose standing EMG activity was hardly noticeable. Ambroz et al66 found the paraspinal EMG activity of the subjects with LBP (matched for age, sex, and body mass index) in a relaxed standing position was 3 times higher than the healthy controls. It is possible that protective reflex muscle contraction may occur in acute conditions where moderate tissue damage has occurred (such as IVD prolapse with acute scoliosis and loss of lordosis), but this seems unlikely to be the mechanism occurring in most cases of LBP. Increased muscle activity in static positions, particularly standing, may be better explained by a combination of voluntary guarding and an altered CNS strategy that causes muscles to behave in ‘‘pain mode,’’ as suggested by Zedka et al.63 While these
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studies lend support to the proposal of muscle overactivity being associated with LBP and palpable paraspinal abnormalities, there still remains a lack of evidence demonstrating this increased activity in muscles that are detected as tender and abnormal to palpation.
Psychophysiological Response to Pain Flor et al72 have demonstrated that stressful events may trigger very specific muscle hyperactivity patterns in individuals with chronic pain. When volunteers with chronic LBP discussed stressful life events or their pain episodes, they responded with marked increases of EMG activity in their lumbar paraspinal musculature but not when reciting nonstressful tasks such as the alphabet or mental arithmetic. Flor et al72 interpreted this as a symptom-specific muscular response stereotypy to personally relevant stress. In a later study, Flor et al73 recorded EMG responses from subjects with LBP, subjects with temporomandibular pain, and healthy controls and asked them to imagine a stressful event that occurred in the past week or to undertake neutral imagery (sitting at home). Flor et al73 found that there was a significant difference between the subjects with LBP and the controls for left erector spinae activity during the stressful imagery and of masseter activity between the temporomandibular pain patients and controls. The EMG activity was increased at the site of pain but not at distal sites (such as trapezius, biceps, or masseter in the LBP patients). Flor et al73 found there were high variances in the muscles of the LBP subjects, indicating that some responded with very high activity, whereas others showed normal responses. The absolute stress-related EMG changes in microvolts were quite small, but Flor et al73 argued that the stressors were imagined and stressors outside the laboratory may evoke much larger responses. Increased resting muscle activity following mental imagery has also been reported by Stohler et al,74 who compared the effect of experimental jaw muscle pain to the effect of mentally recalling an episode of pain. Both the experimentally produced pain and the imagined pain produced similar significant increases in resting EMG levels of temporalis and masseter muscles. Stohler et al74 noted that the resting EMG increases were very small (0.53-0.70lv in experimental pain and 0.63-0.91lv during imagined pain) relative to maximal contraction and believed that it was excessive to call these muscles ‘‘hyperactive.’’ They doubted the likelihood that such tiny increases would produce further muscle pain. The evidence of symptom-specific psychophysiological responses to stress in chronic pain patients suggests that emotional and psychological mechanisms further modify the CNS strategy in reaction to pain. Although Stohler et al74 questioned the relevance of such small increases in resting muscle activity, it is feasible that this increase in activity may make the muscle feel different to palpation. Furthermore, it seems likely that exposure to chronic pain or recurrent
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episodes of acute pain may produce a stronger stereotypical, psychophysiological response in susceptible individuals. It seems possible that most reports of increased paraspinal EMG activity in LBP patients may be explained as a combination of voluntary guarding behavior65,68 and a change in CNS strategy, producing exaggerated ‘‘pain mode’’ muscle activity to limit excessive or unanticipated movement.63 Emotional and psychological experience of chronic pain may further modify or reinforce this altered CNS strategy to produce stereotypical patterns of guarding activity in response to real or imagined stress. The relevance of this abnormally increased muscle activity to paraspinal regions that are tender and feel abnormal to palpation remains untested, but it is feasible that increased muscle activity may be detectible with palpation and even the act of palpation may provoke further muscle guarding.
CONCLUSION Although there is little direct evidence to support the belief that sustained muscle contraction is a feature of intervertebral dysfunction, the concept of protective muscle spasm appears plausible. Reflex multifidus muscle contraction has been demonstrated following electrical and mechanical stimulation of deep spinal structures in animals, and such a reflex has been demonstrated to exist in humans. Additionally, experimental muscle inflammation has been demonstrated to produce increased fusimotor activity and reflex-mediated muscle stiffness. Increased paraspinal muscle activity has been observed in LBP patients during full flexion, static postures, and as a reaction to stressful imagery. It appears that while voluntary guarding behavior may be responsible for increased activity in some patients, increased muscle activity is, in part, due to a nonvoluntary change in CNS control, a proposed ‘‘pain mode’’ strategy in response to pain originating from any spinal structure. There is evidence to support the proposal of abnormally increased paraspinal muscle activity as a consequence of spinal injury. Similar changes to those found in LBP patients may occur in the muscles adjacent to intervertebral injury and produce the commonly reported clinical findings of tenderness and altered tissue texture at a single intervertebral level. What must follow, however, is direct evidence of increased EMG activity associated with the detection of tender and abnormal to palpation paraspinal regions.
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